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Biomedical subjects

R Zelis

Publications and source records attributed to R Zelis.

At least 109 records · Page 6Linked to original sources
PubMed1980

Validation of dynamic radiography in the dog and evaluation of ischemic dyssynergy.

If a collimated radiation detector (sodium iodide crystal) and a collimated X-ray source are positioned at right angles, scattered radiation will be sensed and the detector will generate a signal as tissue enters and leaves the "sensitive volume" formed by the intersection of the field of view of the detector and incident beam. This technique, called dynamic radiography, was used to identify and quantify the components of epicardial motion in anesthetized open-chested dogs. The data so obtained were validated by two independent optical methods: biplane cinematography and a technique that measures the shadow cast by the heart using a light beam-cadmium sulfide photocell. Displacement measured by dynamic radiography appeared to be the time integral of the scalar product of the velocity vector and the vector normal to the surface area within the sensitive volume, i.e., that component of displacement of myocardial mass that was perpendicular to the surface of the myocardium. In other words, the dynamic radiographic signal was proportional to the mass of tissue within the sensitive volume. Good agreement in terms of absolute motion, its direction, and phase was noted between predicted dynamic radiographic signals and those observed. Thus validated, this technique was found to be reliable in quantifying motion abnormalities produced by acute coronary ligation.

Animals↗
PubMed1980

alpha-Stimulation protects exercise increment in skeletal muscle oxygen consumption.

Oxygen consumption (VO2) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5% P0) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO2 were evaluated at rest (Qc and VO2c), after 5 min of exercise (Qe and VO2e) and after 5 more min of exercise with either NE or MO (Qt and VO2t). Data were normalized and plotted as the VO2e-VO2t)/(VO2c-VO2e) vs. (Qe-Qt)/(Qc-Qe) and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P less than 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced in VO2 was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO2 was secondary to a beta-adrenergic-receptor-mediated of skeletal muscle metabolic processes, the experiments were repeated in the presence of beta-blockade with propranolol. In the presence of beta-blockade, the effects of NE on skeletal muscle VO2 were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.

Animals↗
PubMed1980

Diltiazem: lack of myocardial beta-adrenergic receptor-binding capacity.

It has been suggested that the mechanism of action of the calcium blocker diltiazem (DZ) is via beta-receptor blockade. In order to test this hypothesis, the effects of DZ on the competitive binding of 3H-dihydroalprenolol (3H-DHA) to myocardial beta-receptors were evaluated and compared to those of a known beta-receptor agonist. Preliminary validation studies indicate that binding sites for 3H-DHA exhibit stereospecificity for isoproterenol (IP) (l-IP>d-IP) and show greater affinity for l-epinephrine compared to l-norepinephrine. In order to test the binding capacity of DZ to beta-adrenergic receptors, binding-concentration relationships were constructed for 3H-DHA (3--60 nM) in the presence of no drugs, l-IP (10(-4) M), or DZ (2.2 x 10(-6) M). 3H-DHA binding was significantly inhibited over the entire concentration range by 1-IP but was unaffected by the other conditions. This study was repeated using two different concentrations of DZ (2.2 x 10(-5) and 2.2 x 10(-7) M) with a similar lack of inhibition of 3H-DHA binding. These data indicate that DZ does not bind to myocardial beta-receptors and, therefore, does not appear to act via a beta-receptor-blocking activity.

Animals↗
PubMed1979

Pericardial-fluid complement: normal values.

Reports of low pericardial-fluid complement levels in systemic lupus erythematosus and rheumatoid arthritis have been difficult to interpret, as few data are available to describe complement concentrations in patients without pericardial disease. The authors therefore determined normal values under standardized conditions of collection, storage, and assay. The normal ranges for pericardial-fluid C3, C4, and total hemolytic complement were 35-127 mg/dl, 6.3-23 mg/dl, and 1.9-9.1 CH50 units, respectively. Storage at -20 C resulted in a 50% reduction in values. Hence, storage at -70 C is recommended. As the level of pericardial-fluid total hemolytic complement is normally low, caution is needed in interpreting its apparent reduction in various immunologic diseases.

Complement C3↗
PubMed1979

Cardiovascular response to acute aquatic and treadmill exercise in the untrained rat.

The cardiovascular effects of acute aquatic (AE) and treadmill (TE) exercise were determined in untrained adult male Sprague-Dawley rats. Animals were exercised to exhaustion or for a maximum of 5 min with either exercise mode and data collected during the last minute of exercise were compared to preexercise rest data. Heart rate and cardiac output increased only with TE; arterial pressure remained stable during both protocols. Regional blood flow was determined by the radioactive microsphere technique. Coronary flow increased only with TE. Skeletal muscle flow, determined in six muscle groups, increased more with TE (97 to 587%) than with AE (-44 to 260%) (flow in the quadriceps group decreased during AE). Flow to the skin and splanchnic regions decreased; cerebral flow increased in both groups. Blood gas data suggest lactic acidosis and hyperventilation only with TE. These data indicate that 1) the cardiovascular effects of acute, exhaustive bouts of AE and TE in the rat are not comparable, and 2) the hemodynamic changes occurring with exhaustive TE in rat, as in man, involve a shunting of blood to the regions of demand and away from the nonessential circulations.

Abdomen↗
PubMed1979

Cage size and exercise affects infarct size in rat after coronary artery cauterization.

Left coronary occlusion in the rat was performed by cornary artery cauterization. A small amount of myocardial damage at the site of occlusion was noted, and myocardial infarction occurred in the distal distribution of the obstructed coronary. The effects of cage size and level of physical activity on estimated infarct size (as measured by creatine kinase depletion) 48 h after occlusion were determined. Isolation in small cages and moderate treadmill exercise resulted in an approximate doubling of the amount of infarction when compared to grouping of rats in large cages. Mild exercise did not increase infarct size. Total urinary catecholamines in normal rats placed in small cages for 48 h were elevated when compared to unconfined rats in larger cages. Cornary artery occlusion by cauterization is an easily performed technique. Cage size and level of activity (and their effects on sympathoadrenal function) are important independent determinations of infarct extent after coronary occlusion in the rat.

Animals↗
PubMed1979

Pericardial effusions in sarcoidosis.

A case of sarcoid pericarditis is presented. The associated pericardial effusion was a transudate with a low complement level. Investigating the prevalence of pericardial effusions in sarcoid by echocardiography, we found small effusions in 19 percent of 48 consecutive patients with sarcoid. Additionally, ten previously reported cases of symptomatic parietal pericardial sarcoid are reviewed.

Female↗
PubMed1979

Echocardiographic assessment of mitral stenosis by the left atrial emptying index.

Echocardiograms were performed in 35 patients prospectively with mitral stenosis to determine the usefulness of the left atrial emptying index (AEI) in estimating mitral valve orifice area (MVOA). Twnety-five control patients without evidence of cardiac disease had an AEI of 0.91 +/- 0.01. In the mitral stenosis group, the mean AEI was 0.47 +/- 0.09, with Gorlin and Gorlin calculated MVOAs of 1.44 +/- 0.56. There was close correlation between the AEI and MVOA (r = 0.93). The AEI did not correlate well with the left atrial size (r = 0.10), or the EF slope of the mitral valve (r = 0.20). The AEI was useful in separating patients with mitral stenosis into mild, moderate, and severe groups. Twelve out of 12 patients with severe mitral stenosis (MVOA less than or equal to 1.0 sq cm) had an AEI of less than or equal to 0.42. Ten out of 13 patients with moderate mitral stenosis (MVOA of 1.1--1.5 sq cm) had an AEI of 0.43 to 0.51. Eight out of ten patients with mild mitral stenosis (MVOA greater than or equal to 1.6 sq cm) had an AEI of greater than or equal to 0.52. The overall predictive value of the AEI in subclassifying the severity of mitral stenosis was 86 percent. In conclusion, the AEI appears to be a sensitive index in estimating MVOA in mitral stenosis.

Adult↗
PubMed1978

Effects of morphine sulfate on human coronary blood flow.

Because morphine causes coronary vasoconstriction in conscious dogs, human coronary blood flow was measured with the thermodilution technique before and after administration of morphine sulfate, 0.2 mg/kg body weight (maximum 15 mg) intravenously, in 10 patients to determine if the canine experience is clinically applicable. Coronary blood flow increased from a baseline value of 104.4 +/- 13.4 (mean +/- standard error of the mean) to 113.0 +/- 17.4 ml/min (difference not significant) 15 minutes after the administration of morphine. Baseline coronary vascular resistance was 1.14 +/- 0.19 mm Hg/ml/min; 15 minutes after morphine administration the resistance value was 1.02 +/- 0.17 (P less than 0.025). There was no significant change between baseline values and values 15 minutes after morphine administration in systemic mean arterial pressure (98.2 +/- 5.3 to 92.8 +/- 4.7 mm Hg); heart rate (69.5 +/- 3.5 to 72.6 +/- 3.4 beats/min), left ventricular ejection time (0.345 +/- 0.009 to 0.342 +/- 0.007 second) or tension-time index (2,324 +/- 128 to 2,291 +/- 149 mm Hg/sec per min). The slight coronary vasodilation noted after morphine administration in this study is in marked contrast to the significant coronary vasoconstriction demonstrated in the unanesthetized dog.

Adult↗